ArticleInfection and immunity2015
The Candida albicans ATO Gene Family Promotes Neutralization of the Macrophage Phagolysosome.
Article in Infection and immunity, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 56 citations in OpenAlex.
- Expansion, functional diversification, and gene fusion events in the Ato protein family.iScience · 2026Article
- Review
- Molecular Triggers of Yeast Pathogenicity in the Yeast-Host Interactions.Current issues in molecular biology · 2025Review
- ThemBio · 2025Article
- Coordinated regulation of pH alkalinization by two transcription factors promotes fungal commensalism and pathogenicity.Nature communications · 2025Article
- IRE1α promotes phagosomal calcium flux to enhance macrophage fungicidal activity.Cell reports · 2025Article
- Hyphal swelling induced in the phagosome of macrophages.Fungal biology · 2024Article
- Non-canonical activation of IRE1α duringbioRxiv : the preprint server for biology · 2024Article
- An integrated transcriptomic and metabolomic approach to investigate the heterogeneousBiofilm · 2023Article
- "Under Pressure" - How fungi evade, exploit, and modulate cells of the innate immune system.Seminars in immunology · 2023Review
- The Candida glabrata Parent Strain Trap: How Phenotypic Diversity Affects Metabolic Fitness and Host Interactions.Microbiology spectrum · 2023Article
- Host-directed therapy for bacterial infections -Modulation of the phagolysosome pathway.Frontiers in immunology · 2023Review
- Uncovering Novel Plasma Membrane Carboxylate Transporters in the YeastJournal of fungi (Basel, Switzerland) · 2022Article
- Amino Acid Sensing and Assimilation by the Fungal PathogenPathogens (Basel, Switzerland) · 2021Review
- Inflammasome-mediated GSDMD activation facilitates escape of Candida albicans from macrophages.Nature communications · 2021Article
- Deletion of theFrontiers in cellular and infection microbiology · 2021Article
- Glutamate dehydrogenase (Gdh2)-dependent alkalization is dispensable for escape from macrophages and virulence of Candida albicans.PLoS pathogens · 2020Article
- Carboxylic Acid Transporters inmBio · 2020Review
- Adapting to survive: How Candida overcomes host-imposed constraints during human colonization.PLoS pathogens · 2020Review
- The Paralogous Transcription Factors Stp1 and Stp2 of Candida albicans Have Distinct Functions in Nutrient Acquisition and Host Interaction.Infection and immunity · 2020Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Candida albicans is an opportunistic human fungal pathogen that causes a variety of diseases, ranging from superficial mucosal to life-threatening systemic infections, the latter particularly in patients with defects in innate immune function. C. albicans cells phagocytosed by macrophages undergo a dramatic change in their metabolism in which amino acids are a key nutrient. We have shown that amino acid catabolism allows the cell to neutralize the phagolysosome and initiate hyphal growth. We show here that members of the 10-gene ATO family, which are induced by phagocytosis or the presence of amino acids in an Stp2-dependent manner and encode putative acetate or ammonia transporters, are important effectors of this pH change in vitro and in macrophages. When grown with amino acids as the sole carbon source, the deletion of ATO5 or the expression of a dominant-negative ATO1(G53D) allele results in a delay in alkalinization, a defect in hyphal formation, and a reduction in the amount of ammonia released from the cell. These strains also form fewer hyphae after phagocytosis, have a reduced ability to escape macrophages, and reside in more acidic phagolysosomal compartments than wild-type cells. Furthermore, overexpression of many of the 10 ATO genes accelerates ammonia release, and an ato5Δ ATO1(G53D) double mutant strain has additive alkalinization and ammonia release defects. Taken together, these results indicate that the Ato protein family is a key mediator of the metabolic changes that allow C. albicans to overcome the macrophage innate immunity barrier.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.